James A. Radosevich, PhD; Department of Oral Medicine and Diagnostic Sciences, College of Dentistry, University of Illinois at Chicago
Cancer Biology | Cell and Developmental Biology | Dentistry | Genetics | Genetics and Genomics | Life Sciences | Medicine and Health Sciences | Oral Biology and Oral Pathology
Gene chip analysis of ten HNO adapted cell lines (Squamous cells: SCC-016, SCC-040, SCC-056, SCC-114, SCC-116; Adenocarcinomas: A549, BT20, Hs578, MCF7, and T47D) was carried out. Known pseudogenes were identified in each line, as well as their coding counterparts.
The adenocarcinoma cell lines had no up regulated pseudogenes, while they had the following down regulated pseudogenes: RP6-159A1.2, RP11-255N24.3, AC004490.1, LDHBP, RP11-572H4.2. The squamous cell carcinomas (SCCs) had the following up regulated pseudogenes: RPL37AP1, AC138972.1, RP11-641D5.1, AC005534.6, AC022431.1, RPL26P12, and they had these down regulated pseudogenes: RP6-159A1.2, RP11-255N24.3, RBMXP1, RP11-20O23.1, RP11-551G24.2. All cell lines adhered to the hypothesis that an increase in a pseudogene expression also had an increase in the corresponding gene.
The high level of pseudogenes could be due to low levels of microRNA; low expression of microRNA could then be due to high levels of ceRNA. In cases when the pseudogenes increase in expression (possibly due to HNO interference) they, like BRAF, take the functionality of ceRNA which in turn decreases microRNA expression. Although a pseudogene may not have any direct translational significance, it can act as ceRNA to facilitate the over expression of the coding gene in a feedback loop.
Korrapati, K., Kuganeswaran, N. T., Wan, T., & Radosevich, J. A. (2016, March). Role of pseudogenes in cancer stem creation via high nitric oxide (HNO) adaptation. Poster session presented at the meeting of the University of Illinois at Chicago College of Dentistry Clinic & Research Day, Chicago, IL. Retrieved from http://digitalcommons.imsa.edu/student_pr/17/